Description

The Cd274 Knockout CT26 Cell Line is a CRISPR/Cas9-engineered mouse tumor cell model in which the Cd274 gene has been disrupted to eliminate functional PD-L1 expression. Generated in the CT26 host background, this stable knockout line provides an in vitro system for interrogating tumor cell-intrinsic and tumor-immune regulatory functions associated with PD-L1 loss. As CT26 is an epithelial-derived murine colon carcinoma line, this model is suited for studies requiring a genetically defined colorectal tumor context with direct relevance to immune checkpoint biology and therapeutic response.

CT26 is a colon carcinoma cell line derived from BALB/c mouse and is extensively used as a syngeneic transplantation model in immuno-oncology. Its broad adoption reflects its utility in modeling tumor growth, immune regulation, and treatment response in an immunocompetent host setting. In vitro, CT26 cells are frequently used to examine cytokine-driven transcriptional programs, tumor-cell signaling states, and interactions with lymphocytes or other immune effectors. This biological background makes CT26 a valuable platform for investigating mechanisms of immune evasion and adaptive immune resistance relevant to colorectal cancer and other solid tumors.

Cd274 encodes PD-L1, an inducible transmembrane ligand that binds PDCD1 (PD-1) on activated T cells and suppresses T-cell receptor signaling, IL2 production, IFNG production, proliferation, and CD8+ cytotoxic function. In tumor cells, CD274 expression is strongly regulated by IFNG through IFNGR1/IFNGR2, JAK1, JAK2, STAT1, and IRF1, and can also be modulated by TNF-NFKB1-RELA signaling, EGFR, PI3K-AKT-MTOR, MAPK signaling, and HIF1A-dependent programs. PD-L1 stability and surface abundance are further influenced by interacting factors including CMTM6 and CMTM4, while CD80 represents an additional relevant binding partner in immune-regulatory settings. Through these signaling relationships, CD274 functions at the interface of antigen presentation, inflammatory signaling, and tumor-immune interaction.

Loss of Cd274 in the CT26 background is therefore mechanistically informative for separating checkpoint-mediated immune suppression from other tumor-cell signaling outputs. In this host context, the knockout can support analysis of how IFN-gamma-induced transcriptional responses are coupled or uncoupled from PD-L1-dependent immune inhibition, and how tumor cells engage adaptive immune resistance pathways in the absence of this ligand. The model is also useful for studying pathway dependency downstream of JAK-STAT, NF-kB, PI3K-AKT, or MAPK inputs without confounding effects from intact PD-1/PD-L1 checkpoint signaling.

This cell line can be applied in flow cytometry, western blotting, RT-qPCR, RNA-seq, and immunofluorescence workflows to characterize Cd274 loss and associated transcriptional or signaling changes, including phospho-STAT1 responses after IFNG stimulation. In tumor-immune co-culture systems, it enables direct assessment of PD-L1-dependent effects on T-cell activation, cytokine release, and cytotoxicity using cytokine measurement and killing assays. It is also appropriate for reporter assays, drug sensitivity studies, and combination treatment experiments evaluating checkpoint-related resistance mechanisms, as well as in vivo syngeneic tumor studies in BALB/c-compatible settings. Researchers may contact Ascent Research for additional technical information, product details, or related gene-edited cell models.